Target intelligence / Profile preview

Tumor suppressor candidate 3 (TUSC3)

Target
TUSC3
Molecular classification
Enzyme (subunit of oligosaccharyltransferase complex), Transporter (magnesium transporter), Other (endoplasmic reticulum integral membrane protein)
01

Overview

Tumor suppressor candidate 3 (TUSC3) is an integral membrane protein of the endoplasmic reticulum and a non-catalytic subunit of the oligosaccharyltransferase complex, which is pivotal for N-linked glycosylation of proteins—a modification important for protein folding, stability, and function[1][2][4]. TUSC3 also facilitates magnesium transport across membranes, contributing to cellular magnesium homeostasis[2][4]. In cancer biology, TUSC3 is frequently deleted, mutated, or epigenetically silenced in multiple epithelial malignancies (notably prostate, ovarian, colorectal, and breast cancers), with its loss promoting cell proliferation, migration, invasion, and resistance to ER stress-induced apoptosis; these functions underline its role as a tumor suppressor[1][3][4]. Additionally, loss-of-function mutations in TUSC3 are a cause of autosomal recessive intellectual disability[2][4]. Currently, no approved drugs directly target TUSC3, but its loss is recognized as a clinically relevant biomarker for cancer progression and prognosis through detection of gene deletion or promoter hypermethylation[2][3].

Other names
Dolichyl-diphosphooligosaccharide--protein glycosyltransferase subunit TUSC3N33Oligosaccharyl transferase subunit TUSC3MGC13453OST3AMRT7MagT2SLC58A2Magnesium uptake/transporter TUSC3Protein N33D8S1992M33MRT22oligosaccharyltransferase 3 homolog A (S. cerevisiae)
02

Mechanism of action

Not directly drug-targeted (no approved drugs), but as a tumor suppressor, loss or silencing can contribute to drug resistance or sensitivity to agents inducing ER stress

03

Biological functions

N-glycosylation of nascent proteinsMagnesium ion transport and homeostasisRegulation of endoplasmic reticulum stress responseCell proliferation regulationInduction of apoptosis (as tumor suppressor)
04

Disease associations

Cancer (prostate, breast, colorectal, ovarian, pancreatic, oral squamous)Neurodevelopmental disorders (autosomal recessive intellectual disability)Other (potential role in other epithelial-derived malignancies)
05

Safety considerations

Therapeutic modulation may risk ER stress homeostasis and normal cell glycoprotein processingMutation or complete loss leads to intellectual disability and developmental delay
06

Biomarkers

Promoter methylation of TUSC3 (as a prognostic biomarker in several cancers, especially ovarian and colorectal)Downregulation or deletion associated with tumor progression and poor prognosis

Beyond the preview

Go deeper on Tumor suppressor candidate 3 (TUSC3).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Tumor suppressor candidate 3 (TUSC3).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call